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Am J Reprod Immunol. 2009 Mar;61(3):190-5. doi: 10.1111/j.1600-0897.2008.00681.x.

Effect of sulfasalazine on basal and bacteria-stimulated interleukin-8 production by endocervical epithelial cells.

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1
Department of Obstetrics, Gynecology and Reproductive Sciences, UMDNJ-Robert Wood Johnson Medical School/Robert Wood Johnson University Hospital, New Brunswick, NJ, USA. mpeltier@winthrop.org

Abstract

PROBLEM:

Sulfasalazine (SASP) inhibits lipopolysaccharide-induced nuclear-factor kappa B activation and interleukin-8 (IL-8) production by cultured explants of placenta, amnion and choriodecidua. Bacteria-induced IL-8 production in the cervix is a potential mechanism for premature cervical ripening that may lead to preterm birth. Our objective was to determine if SASP inhibits IL-8 production by endocervical cells stimulated with bacterial pathogens associated with preterm birth.

METHOD OF STUDY:

Human endocervical cells were incubated with 0-1.6 mm SASP and then stimulated with Ureaplasma parvum, Escherichia coli, or Gardnerella vaginalis. Conditioned medium was then harvested and production of IL-8 was quantified by ELISA. Viability of the cells was ascertained at the end of the experiment with the MTT-assay.

RESULTS:

At the highest concentration tested (1.6 mm), SASP significantly inhibited IL-8 production by cultures stimulated with E. coli (P < 0.001), U. parvum (P < 0.001), and G. vaginalis (P < 0.001). Viability of the cells, however, was significantly reduced by SASP at 0.8 and 1.6 mm in both the presence and absence of bacteria for all experiments.

CONCLUSION:

Although high concentrations of SASP inhibit IL-8 production by cultures of endocervical cells stimulated with pathogens associated with preterm birth, this effect may be because of toxicity of the antibiotic on the cells.

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